Poisonings

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Chapter 58 Poisonings

Katherine A. O’Donnell, Michele Burns Ewald

Of the more than 2 million human poisoning exposures reported annually to the National Poison Data Systems of the American Association of Poison Control Centers (AAPCC), more than 50% occur in children <6 yr old. Almost all of these exposures are unintentional and reflect the propensity for young children to put virtually anything in their mouths.

More than 90% of toxic exposures in children occur in the home, and most involve only a single substance. Ingestion accounts for the vast majority of exposures, with a minority occurring via the dermal, inhalational, and ophthalmic routes. Approximately 50% of cases involve nondrug substances, such as cosmetics, personal care items, cleaning solutions, plants, and foreign bodies. Pharmaceutical preparations account for the remainder of exposures, and analgesics, topical preparations, cough and cold products, and vitamins are the most commonly reported categories.

More than 85% of poisoning exposures in children <6 yr can be managed without direct medical intervention, either because the product involved is not inherently toxic or the quantity of the material involved is not sufficient to produce clinically relevant toxic effects (Table 58-1). However, a number of substances are potentially highly toxic to toddlers in small doses (Table 58-2). Fatalities often result from carbon monoxide, iron, analgesics, hydrocarbons, cardiovascular drugs, antidepressants, and pesticides. Although the majority of exposures occur in children <6 yr, only 2.8% of the reported deaths occur in this age group. In addition to the exploratory nature of ingestions in young children, product safety measures, poison prevention education, early recognition of exposures, and around-the-clock access to regionally based poison control centers all contribute to the favorable outcomes in this age group.

Table 58-1 COMMON NONTOXIC AND MINIMALLY TOXIC * PRODUCTS

Abrasives

Antacids, non-salicylate-containing

Antibiotics, topical

Antifungals, topical

Ballpoint pen ink

Bathtub floating toys

Bath oil (unless aspirated)

Body conditioners

Bubble bath soap

Calamine lotion

Candles (beeswax or paraffin)

Caps (toy pistols, potassium chlorate)

Chalk (calcium carbonate)

Children’s toy cosmetics

Clay (modeling)

Contraceptives (oral) without iron

Corticosteroids, topical

Cosmetics

Crayons

Dehumidifying packets (e.g., silica)

Deodorants, underarm

Fabric softeners

Fertilizers (no insecticides or herbicides)

Detergents: hand, dishwashing

Diaper rash creams and ointments

Fishbowl additives

Glow products (glowsticks)

Glues and paste

Golf ball (core can cause mechanical injury)

Grease

Hand lotions and creams

Hydrogen peroxide (medicinal 3%)

Incense

Indelible markers

Ink (black or blue, nonpermanent)

Iodophil disinfectants (unless the person is allergic)

Laxatives

Lipstick

Lozenges (without anesthetics)

Lubricating oils (unless aspirated)

Mineral oil (unless aspirated)

Modeling compound (Play-Doh)

Newspaper (chronic ingestion can result in lead poisoning)

Paint, indoor latex, water-based

Paints, watercolor

Pencil lead (graphite, coloring)

Petroleum jelly (Vaseline)

Plant food (no insecticides or herbicides)

Polaroid picture coating fluid

Putty

Rubber cement

Shampoo

Shaving creams and lotions

Silica gel

Soap and soap products (noncaustic)

Spackle

Starch

Sunscreen

Sweetening agents (saccharin, aspartame)

Toothpaste (with and without fluoride)

Warfarin rodenticides (<0.5%)

Watercolor paints

Zinc oxide

* The potential for toxicity depends on the magnitude and amount of exposure. These agents are considered nontoxic or minimally toxic for mild to moderate exposure. The potential for toxicity increases with increased amount of exposure.

Table 58-2 MEDICATIONS POTENTIALLY TOXIC TO YOUNG CHILDREN IN SMALL DOSES *

SUBSTANCE	TOXICITY
Antimalarials (chloroquine, quinine)	Seizures, cardiac arrhythmias
Benzocaine	Methemoglobinemia
β-Blockers (lipid-soluble β-blockers [e.g., propranolol] are more toxic than water-soluble β-blockers [e.g., atenolol])	Bradycardia, hypotension, hypoglycemia
Calcium channel blockers	Bradycardia, hypotension, hyperglycemia
Camphor	Seizures
Clonidine	Lethargy, bradycardia, hypotension
Diphenoxylate and atropine (Lomotil)	CNS depression, respiratory depression
Hypoglycemics, oral (sulfonylureas and meglitinides)	Hypoglycemia, seizures
Lindane	Seizures
Monoamine oxidase Inhibitors	Hypertension followed by delayed cardiovascular collapse
Methyl salicylates	Tachypnea, metabolic acidosis, seizures
Opioids (especially methadone, lomotil and suboxone)	CNS depression, respiratory depression
Phenothiazines (chlorpromazine, hioridazine)	Seizures, cardiac arrhythmias
Theophylline	Seizures, cardiac arrhythmias
Tricyclic antidepressants	CNS depression, seizures, cardiac arrhythmias, hypotension

CNS, central nervous system.

* “Small dose” typically implies 1 or 2 pills or 5 mL.

Poison prevention education should be an integral part of all well child visits, starting at the 6-mo visit. Counseling parents and other caregivers about potential poisoning risks, how to poison-proof a child’s environment, and what to do if an ingestion or exposure occurs diminishes the likelihood of serious morbidity or mortality. Poison prevention education materials are available from the American Academy of Pediatrics and regional poison control centers. A network of poison control centers exists in the U.S., and anyone at any time can contact a regional poison center by calling a toll-free number: 1-800-222-1222. Parents should be encouraged to share this number with grandparents, relatives, and any other caregivers.

Poisoning exposures in children 6-12 yr old are much less common, involving only ~ 6% of all reported pediatric exposures. A second peak in pediatric exposures occurs in adolescence. Exposures in the adolescent age group are primarily intentional (suicide or abuse or misuse of substances) and thus often result in more severe toxicity (see Chapter 108). Families should be informed and given anticipatory guidance that over-the-counter (OTC) and prescription medications and even household products (e.g., inhalants) are common sources of adolescent exposures. Adolescents (ages 13-19 yr) accounted for 56 of the 102 reported poison-related pediatric deaths in 2007. Pediatricians should be aware of the signs of drug abuse or suicidal ideation in this population and should aggressively intervene (Chapter 108).

Approach to the Poisoned Patient

The initial approach to the patient with a witnessed or suspected poisoning should be no different than that in any other sick child, starting with stabilization and rapid assessment of the airway, breathing, circulation, and mental status (Chapter 62). A serum dextrose concentration should be obtained early in the evaluation of any patient with altered mental status. A targeted history and physical examination serves as the foundation for a thoughtful differential diagnosis, which can then be further refined through laboratory testing and other diagnostic studies.

Initial Evaluation

History

Obtaining an accurate problem-oriented history is of paramount importance. Intentional poisonings (suicide attempts; abuse or misuse) are typically more severe than unintentional, exploratory ingestions. In patients without a witnessed exposure, historical features such as age of the child (toddler or adolescent), acute onset of symptoms without prodrome, sudden alteration of mental status, multiple system organ dysfunction, or highs levels of household stress should suggest a possible diagnosis of poisoning.

Description of the Exposure

For household and workplace products, names (brand, generic, chemical) and specific ingredients, along with their concentrations, can often be obtained from the labels. Poison control center specialists can also help to identify possible ingredients and review the potential toxicities of each component. In cases of suspected ingestion, poison center specialists can help identify pills based on markings, shape, and color. If referred to the hospital for evaluation, parents should be instructed to bring the products, pills, and/or containers with them to assist with identifying and quantifying the exposure. If a child is found with an unknown pill in his or her mouth, the history must include a list of all medications in the child’s environment (including medications that grandparents, caregivers, or other visitors might have brought into the house). In the case of an unknown exposure, clarifying where the child was found (e.g., garage, kitchen, laundry room, bathroom, backyard, workplace) can help to generate a list of potential toxins.

Next, it is important to clarify the timing of the ingestion and to obtain some estimate of how much of the substance was ingested. In general, it is better to overestimate the amount ingested in order to prepare for the worst-case scenario. Counting pills or measuring the remaining volume of a liquid ingested can sometimes be useful in generating estimates.

For inhalational, ocular, or dermal exposures, the concentration of the agent and the length of contact time with the material should be determined as well as possible.

Symptoms

Obtaining a description of symptoms experienced after ingestion, including their timing of onset relative to the time of ingestion and their progression, can help to generate a list of potential toxins and to predict the severity of the ingestion. Coupled with physical exam findings, reported symptoms assist practitioners in identifying toxidromes or recognized poisoning syndromes suggestive of poisoning from specific substances or classes of substances (Tables 58-3 and 58-4).

Table 58-3 HISTORICAL AND PHYSICAL FINDINGS IN POISONING

SIGN	TOXIN
ODOR
Bitter almonds	Cyanide
Acetone	Isopropyl alcohol, methanol, paraldehyde, salicylates
Alcohol	Ethanol
Wintergreen	Methyl salicylate
Garlic	Arsenic, thallium, organophosphates, selenium
OCULAR SIGNS
Miosis	Opioids (except propoxyphene, meperidine, and pentazocine), organophosphates and other cholinergics, clonidine, phenothiazines, sedative-hypnotics, olanzapine
Mydriasis	Atropine, cocaine, amphetamines, antihistamines, TCAs, carbamazepine, serotonin syndrome, PCP, LSD, post-anoxic encephalopathy
Nystagmus	Phenytoin, barbiturates, sedative-hypnotics, alcohols, carbamazepine, PCP, ketamine, dextromethorphan
Lacrimation	Organophosphates, irritant gas or vapors
Retinal hyperemia	Methanol
CUTANEOUS SIGNS
Diaphoresis	Organophosphates, salicylates, cocaine and other sympathomimetics, serotonin syndrome, withdrawal syndromes
Alopecia	Thallium, arsenic
Erythema	Boric acid, elemental mercury, cyanide, carbon monoxide, disulfuram, scombroid, anticholinergics
Cyanosis (unresponsive to oxygen)	Methemoglobinemia (e.g., benzocaine, dapsone, nitrites, phenazopyridine), amiodarone, silver
ORAL SIGNS
Salivation	Organophosphates, salicylates, corrosives, ketamine, PCP, strychnine
Oral Burns	Corrosives, oxalate-containing plants
Gum lines	Lead, mercury, arsenic, bismuth
GASTROINTESTINAL SIGNS
Diarrhea	Antimicrobials, arsenic, iron, boric acid, cholinergics, colchicine, withdrawal
Hematemesis	Arsenic, iron, caustics, NSAIDs, salicylates
CARDIAC SIGNS
Tachycardia	Sympathomimetics (e.g., amphetamines, cocaine), anticholinergics, antidepressants, theophylline, caffeine, antipsychotics, atropine, salicylates, cellular asphyxiants (cyanide, carbon monoxide, hydrogen sulfide), withdrawal
Bradycardia	β-Blockers, calcium channel blockers, digoxin, clonidine and other central α₂ agonists, organophosphates, opioids, sedative-hypnotics
Hypertension	Sympathomimetics (amphetamines, cocaine, LSD), anticholinergics, clonidine (early), monoamine oxidase inhibitors
Hypotension	β blockers, calcium channel blockers, cyclic antidepressants, iron, phenothiazines, barbiturates, clonidine, theophylline, opioids, arsenic, amatoxin mushrooms, cellular asphyxiants (cyanide, carbon monoxide, hydrogen sulfide), snake envenomation
RESPIRATORY SIGNS
Depressed respirations	Opioids, sedative-hypnotics, alcohol, clonidine, barbiturates
Tachypnea	Salicylates, amphetamines, caffeine, metabolic acidosis (ethylene glycol, methanol, cyanide), carbon monoxide, hydrocarbons
CENTRAL NERVOUS SYSTEM SIGNS
Ataxia	Alcohol, anticonvulsants, benzodiazepines, barbiturates, lithium, dextromethorphan, carbon monoxide, inhalants
Coma	Opioids, sedative-hypnotics, anticonvulsants, cyclic antidepressants, antipsychotics, ethanol, anticholinergics, clonidine, GHB, alcohols, salicylates, barbiturates
Seizures	Sympathomimetics, anticholinergics, antidepressants (especially TCAs, bupropion, venlafaxine), isoniazid, camphor, lindane, salicylates, lead, organophosphates, carbamazepine, tramadol, lithium, ginkgo seeds, water hemlock, withdrawal
Delirium/psychosis	Sympathomimetics, anticholinergics, LSD, PCP, hallucinogens, lithium, dextromethorphan, steroids, withdrawal
Peripheral neuropathy	Lead, arsenic, mercury, organophosphates

PCP, phencyclidine; LSD, lysergic acid diethylamide; TCA, tricylic antidepressants; NSAID, nonsteroidal anti-inflammatory drug; GHB, gamma hydroxybutyrate.

Table 58-4 RECOGNIZABLE POISON SYNDROMES

Past Medical History

Underlying diseases can make a child more susceptible to the effects of a toxin. Concurrent drug therapy can also increase susceptibility because certain drugs can interact with the toxin. Pregnancy is a common precipitating factor in adolescents’ suicide attempts and can influence both evaluation of the patient and subsequent treatment. A history of psychiatric illness can make patients more prone to substance abuse, misuse, or intentional ingestions. A developmental history is important to ensure that the history provided is appropriate for the child’s developmental stage (e.g., a report of a 6 mo old picking up a large container of laundry detergent and drinking it should raise a red flag).

Social History

Understanding the child’s social environment helps to identify potential sources of exposures (caregivers, visitors, grandparents, recent parties or social gatherings) and environmental stressors (new baby, parent’s illness, financial stress) that might have contributed to the ingestion. Unfortunately, some poisonings occur in the setting of serious neglect or intentional abuse.

Physical Examination

A targeted physical exam is important to identifying the toxin and assessing the severity of the exposure. Initial efforts should be directed toward assessing and stabilizing the airway, breathing, circulation, and mental status. Once one has ensured that the airway is secure and the patient is stable from a cardiopulmonary standpoint, a more extensive physical exam can help to identify characteristics of specific toxins or classes of toxins.

In the poisoned patient, the key features of the physical exam are the vital signs, mental status, pupils (size, reactivity, nystagmus), skin, bowel sounds, and odors. Together, these findings might suggest a toxidrome (see Tables 58-3 and 58-4) that can guide the differential diagnosis and initial management.

Laboratory Evaluation

For select intoxications (salicylates, some anticonvulsants, acetaminophen, iron, digoxin, methanol, lithium, theophylline, ethylene glycol, carbon monoxide), quantitative blood concentrations are integral to confirming the diagnosis and formulating a treatment plan. For most exposures, qualitative measurement is not possible and is not likely to alter management. Comprehensive, qualitative drug screens vary widely in their ability to detect toxins and generally add little information to the clinical assessment, particularly if the agent is known and the patient’s symptoms are consistent with that agent. If a drug screen is ordered, it is important to examine both serum and urine and to know that the components screened for in a toxicology screen, and the lower limits of detection, vary from hospital to hospital. In addition, the interpretation of most drug screens is hampered by false-positive and false-negative results. Most standard urine opiate screens won’t be positive after ingestion of a synthetic opioid (e.g., methadone, suboxone). Although the presence of some drugs (e.g., marijuana) might not be clinically useful, it can identify use of “gateway drugs” and an adolescent at risk for substance abuse. Consultation with a medical toxicologist can be helpful in interpreting drug screens and ordering specific drug levels or metabolites that can aid in patient management.

Toxicology screens may be indicated in the assessment of the neglected or allegedly abused child, because a positive toxicology screen can add substantial weight to a claim of abuse or neglect. In these cases and any case with medicolegal implications, any positive screen must be confirmed with gas chromatography/mass spectroscopy (GC/MS), which is considered the gold standard measurement for legal purposes.

Acetaminophen is a widely available medication and a commonly detected co-ingestant with the potential for severe toxicity. Given that patients might initially be asymptomatic and might not report acetaminophen as a co-ingestant, an acetaminophen level should be checked in all patients who present after an intentional exposure or ingestion. Furthermore, in any clinical situation with potential medicolegal implications, any positive drug screen should be confirmed by a more sensitive and specific method (typically GC/MS).

Based on the clinical presentation, additional labs tests that may be helpful include electrolytes and renal function (an elevated anion gap suggests a number of ingestions), serum osmolarity (toxic alcohols), complete blood count, liver function tests, urinalysis (crystals), co-oximetry, and a serum creatine kinase level (Table 58-5).

Table 58-5 SCREENING LABORATORY CLUES IN TOXICOLOGIC DIAGNOSIS

ANION GAP METABOLIC ACIDOSIS (MNEMONIC = MUDPILES)

Methanol, metformin

Uremia*

Diabetic ketoacidosis

Paraldehyde, phenformin

Isoniazid, iron, massive ibuprofen

Ethylene glycol, ethanol

Lactic Acidosis (i.e. cyanide, carbon monoxide)

Salicylates

ELEVATED OSMOLAR GAP

Alcohols: ethanol, isopropyl, methanol, ethylene glycol

HYPOGLYCEMIA (MNEMONIC = HOBBIES)

Hypoglycemics, oral: sulfonylureas, meglitinides

Other: quinine, unripe ackee fruit

HYPERGLYCEMIA

Calcium channel blockers

Caffeine

HYPOCALCEMIA

Ethylene glycol

Fluoride

RHABDOMYOLYSIS

Diphenhydramine, doxylamine

Neuroleptic malignant syndrome

Statins

Mushrooms (tricholoma equestre)

Any toxin causing prolonged immobilization (e.g., opioids) or excessive muscle activity or seizures (e.g., sympathomimetics)

RADIOPAQUE SUBSTANCE ON KUB (MNEMONIC = CHIPPED)

Chloral hydrate, calcium carbonate

Heavy metals (lead, zinc, barium, arsenic, lithium, bismuth, as in Pepto-Bismol)

Iron

Phenothiazines

Play-Doh, potassium chloride

Enteric-coated pills

Dental amalgam

KUB, kidney-ureter-bladder radiograph.

Additional Diagnostic Testing

An electrocardiogram (ECG) is a quick and noninvasive bedside test that can yield important clues to diagnosis and prognosis. Toxicologists pay particular attention to the ECG intervals (Table 58-6). A widened QRS interval suggests blockade of fast sodium channels, as may be seen after ingestion of tricyclic antidepressants, diphenhydramine, cocaine, propoxyphene, and carbamazepine, among others. A widened QTc interval suggests effects at the potassium rectifier channels and portends a risk of torsades de pointes.

Table 58-6 ELECTROCARDIOGRAPHIC FINDINGS IN POISONING

PR INTERVAL PROLONGATION

Digoxin

Lithium

QRS PROLONGATION

Tricyclic antidepressants

Diphenhydramine

Carbamazepine

Cardiac glycosides

Chloroquine, hydoxychloroquine

Cocaine

Lamotrigine

Quindine, quinine, procainamide, disopyramide

Phenothiazines

Propoxyphene

Propranolol

Bupropion, venlafaxine (rare)

QTc PROLONGATION*

Amiodarone

Antipsychotics (typical and atypical)

Arsenic

Cisapride

Citalopram and other SSRIs

Clarithromycin, Erythromycin

Disopyramide, Dofetilide, Ibutilide

Fluconazole, ketoconazole, itraconazole

SSRI, selective serotonin reuptake inhibitor.

* This is a select list of important toxins, but other medications are also associated with QTc prolongation.

Chest x-ray may reveal signs of pneumonitis (e.g., hydrocarbon ingestion), pulmonary edema (e.g., salicylate toxicity), or a foreign body. Abdominal x-ray can suggest the presence of a bezoar, demonstrate radiopaque tablets, or reveal drug packets in a body packer. Endoscopy may be useful after significant caustic ingestions. Further diagnostic testing is based on the differential diagnosis and pattern of presentation (Table 58-7).

Table 58-7 DRUGS ASSOCIATED WITH MAJOR MODES OF PRESENTATION

COMMON TOXIC CAUSES OF CARDIAC ARRHYTHMIA

Cyclic antidepressants

CAUSES OF COMA

Cyclic antidepressants

COMMON AGENTS CAUSING SEIZURES (MNEMONIC = CAPS)

Camphor, carbamazepine, carbon monoxide, cocaine, cyanide

Aminophylline, Amphetamine, anticholinergics, antidepressants (cyclic)

Pb (lead) [also lithium], pesticide (organophosphate), phencyclidine, phenol, phenothiazines, propoxyphene

Salicylates, strychnine

* Causes of methemoglobinemia: amyl nitrite, aniline dyes, benzocaine, bismuth subnitrate, dapsone, primaquone, quinones, spinach, sulfonamides.

From Kliegman RM, Mascdante KJ, Jenson HB, editors: Nelson essentials of pediatrics, ed 5, Philadelphia, 2006, Elsevier, p 208.

Principles of Management

The four principles of management of the poisoned patient are decontamination, enhanced elimination, antidotes, and supportive care. Few patients meet criteria for all of these interventions, though clinicians should consider each option in every poisoned patient so as not to miss a potentially lifesaving therapy. Antidotes are available for relatively few poisons (Table 58-8), thus emphasizing the importance of meticulous supportive care and close clinical monitoring.

Table 58-8 COMMON ANTIDOTES FOR POISONING

Poison control centers are staffed by nurses, pharmacists, and physicians specifically trained to provide expertise in the management of poisoning exposures. Parents should be instructed to call the poison control center (1-800-222-1222) for any concerning exposure. Poison specialists can assist parents in assessing the potential toxicity and severity of the exposure. In doing so, they can further determine which children can be monitored at home versus who should be referred to the emergency department (ED) for further evaluation and care. The American Academy of Clinical Toxicology has generated consensus statements for out-of-hospital management of common ingestions (e.g., acetaminophen, iron, selective serotonin reuptake inhibitors) that serve to guide poison center recommendations.

Decontamination

The majority of poisonings in children are due to ingestion, though exposures can also occur via inhalational, dermal and ocular routes. The goal of decontamination is to prevent absorption of the toxic substance. The specific method employed depends on the properties of the toxin itself and the route of exposure. Regardless of the decontamination method used, the efficacy of the intervention decreases with increasing time since exposure. Thus, decontamination should not be routinely employed for every poisoned patient. Instead, careful decisions regarding the utility of decontamination should be made for each patient and should include consideration of the toxicity and pharmacologic properties of the exposure, the route of the exposure, the time since the exposure, and the risks versus the benefits of the decontamination method.

Dermal and ocular decontamination begin with removal of any contaminated clothing and particulate matter, followed by flushing of the affected area with tepid water or normal saline. Treating clinicians should wear proper protective gear when performing irrigation. Flushing for a minimum of 10 to 20 minutes is recommended for most exposures, although some chemicals (e.g., alkaline corrosives) require much longer periods of flushing. Dermal decontamination, especially after exposure to adherent or lipophilic (e.g., organophosphates) agents, should include thorough cleansing with soap and water. Water should not be used for decontamination after exposure to highly reactive agents, such as elemental sodium, phosphorus, calcium oxide, and titanium tetrachloride. After an inhalational exposure, decontamination involves moving the patient to fresh air and administering supplemental oxygen if indicated.

Gastrointestinal (GI) decontamination is a controversial topic among medical toxicologists, with numerous studies documenting marked variability in recommendations. In general, GI decontamination strategies are most likely to be effective in the first hour after an acute ingestion. GI absorption may be delayed after ingestion of agents that slow GI motility (anticholinergic medications, opioids), massive pill ingestions, sustained-release preparations, and ingestions of agents that can form pharmacologic bezoars (e.g., enteric-coated salicylates). Thus, GI decontamination at >1 hr after ingestion may be considered in patients who ingest toxic substances with these properties. Described methods of GI decontamination include induced emesis with ipecac, gastric lavage, cathartics, activated charcoal, and whole-bowel irrigation (WBI). Of these, only activated charcoal and WBI are likely to have significant clinical benefit in management of the poisoned patient.

ANTACIDS

Aluminum hydroxide

BULK-FORMING LAXATIVES

Combination laxatives (e.g., Perdiem)

Psyllium

EXTENDED-RELEASE PRODUCTS

Nifedipine

Procainamide

Verapamil

ION-EXCHANGE RESINS

Sodium polystyrene sulfonate

Calcium polystyrene sulfonate

VITAMIN AND NATURAL PRODUCTS

OTHER MEDICATIONS

Enteric-coated aspirin

Lithium

Salicylic acid

Sucralfate

Enhanced Elimination

Enhancing excretion is only useful for a few toxins; in these cases, enhancing elimination is a potentially lifesaving intervention (e.g., hemodialysis for methanol toxicity).

Multiple-Dose Activated Charcoal

Whereas single-dose activated charcoal is used as a method of decontamination, multiple doses of charcoal (MDAC) can help to enhance the elimination of some toxins. MDAC is typically given as 0.5 g/kg every 4-6 hr (for ≤24 hr) and continued until there is significant clinical improvement, including satisfactory decline of serum drug concentrations. Multiple doses of charcoal enhance elimination via two proposed mechanisms: interruption of enterohepatic recirculation and “GI dialysis,” which uses the intestinal mucosa as the dialysis membrane and pulls toxins from the tissues into the intraluminal space, where they are adsorbed to the charcoal. The AACT/EAPCCT position statement recommends MDAC in managing significant ingestions of carbamazepine, dapsone, phenobarbital, quinine, and theophylline. Many toxicologists consider using MDAC to manage salicylate toxicity that has persistently rising or inadequately falling salicylate levels (suggesting the presence of a pharmacobezoar).

As with single-dose activated charcoal, contraindications to use of MDAC include an unprotected airway and a concerning abdominal exam (e.g., ileus, distention, peritoneal signs); thus the airway and abdominal exam should be assessed before each dose. A cathartic (e.g., sorbitol) may be given with the first dose, but it should not be used with subsequent doses owing to the risk of dehydration and electrolyte derangements.

Urinary Alkalinization

Alkalinizing the urine enhances the elimination of some drugs that are weak acids by forming charged particles that are “trapped” within the renal tubules and thus excreted. Urinary alkalinization is accomplished with a continuous infusion of sodium bicarbonate–containing intravenous fluids, with a goal urine pH of 7.5-8. Alkalinization of the urine is most useful in managing salicylate and methotrexate toxicity. Alkalinization may also be beneficial in managing phenobarbital toxicity, though MDAC is thought to be a superior method of enhancing elimination of phenobarbital.

Serum pH should be closely monitored because a serum pH of >7.55 is potentially dangerous to cellular functions. Other complications of urinary alkalinization include electrolyte derangements, such as hypokalemia and hypocalcemia. This method of enhanced elimination is contraindicated in patients who are unable to tolerate the large volumes of fluid needed to achieve alkalinization, including patients with heart failure, kidney failure, pulmonary edema, or cerebral edema.

Dialysis

Few drugs or toxins are removed by dialysis in amounts sufficient to justify the risks and difficulty of dialysis. Toxins that are amenable to dialysis have the following properties: low volume of distribution (<1 L/kg), low molecular weight, low degree of protein binding, and high degree of water solubility. Examples of toxins for which dialysis may be useful include methanol and ethylene glycol, as well as large symptomatic ingestions of salicylates, theophylline, bromide, or lithium. In addition to enhancing the elimination of the toxin itself, hemodialysis can also be useful to correct severe electrolyte disturbances and acid-base derangements resulting from the ingestion (e.g., metformin-associated lactic acidosis).

Antidotes

Antidotes are available for relatively few toxins (Table 58-11, and see Table 58-8), but early and appropriate use of an antidote is a key element in managing the poisoned patient. Consensus guidelines indicate the important antidotes to stock in facilities that provide emergency care.

Table 58-11 ADDITIONAL ANTIDOTES

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